The Epigenomic Analysis of Human Obesity

Bell, Christopher G.

doi:10.1002/oby.21909

Cited by 48 publications

(45 citation statements)

References 127 publications

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“…Moreover, metabolic challenges, such as caloric or oxygen restriction or even a high-fat diet ( 16 – 19 ), will drive cell fate decisions. Consistent with this, dramatic epigenetic changes have been linked to metabolic disorders, such as obesity, insulin resistance, type-2 diabetes, and cancer ( 20 – 25 ). In this perspective, this review will focus on cofactor families linking nutritional input and metabolism to epigenetic pattern modifications.…”

Section: Introductionmentioning

confidence: 70%

Cofactors As Metabolic Sensors Driving Cell Adaptation in Physiology and Disease

et al. 2017

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Chromatin architectures and epigenetic fingerprint regulation are fundamental for genetically determined biological processes. Chemical modifications of the chromatin template sensitize the genome to intracellular metabolism changes to set up diverse functional adaptive states. Accumulated evidence suggests that the action of epigenetic modifiers is sensitive to changes in dietary components and cellular metabolism intermediates, linking nutrition and energy metabolism to gene expression plasticity. Histone posttranslational modifications create a code that acts as a metabolic sensor, translating changes in metabolism into stable gene expression patterns. These observations support the notion that epigenetic reprograming-linked energy input is connected to the etiology of metabolic diseases and cancer. In the present review, we introduce the role of epigenetic cofactors and their relation with nutrient intake and we question the links between epigenetic regulation and the development of metabolic diseases.

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Section: Introductionmentioning

confidence: 70%

Cofactors As Metabolic Sensors Driving Cell Adaptation in Physiology and Disease

et al. 2017

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“…Obesity is a pro-inflammatory state with a broad impact on health and is the main risk factor for metabolic diseases such as diabetes, with an alarming increase worldwide [ 1 ]. Epigenetic mechanisms such as DNA methylation and regulation by microRNAs (miRs) play a central role in the obesogenic environment [ 2 , 3 ]. Conditions associated with obesity, such as chronic inflammation, hyperglycaemia and hyperlipidaemia, are related to changes in DNA methylation status and gene expression [ 2 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

α-Tocopherol influences glycaemic control and miR-9-3 DNA methylation in overweight and obese women under an energy-restricted diet: a randomized, double-blind, exploratory, controlled clinical trial

et al. 2018

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BackgroundExcess weight is a strong risk factor for the development of dysglycaemia. It has been suggested that changes in the metabolism microRNAs, small non-coding RNAs that regulate gene expression, could precede late glycaemic changes. Vitamin E in turn may exert important functions in methylation and gene expression processes. This study aimed to determine the effect of α-tocopherol on glycaemic variables and miR-9-1 and miR-9-3 promoter DNA methylation in overweight women.MethodsA randomized, double-blind, exploratory, placebo-controlled study was conducted in overweight and obese adult women (n = 44) who ingested synthetic vitamin E (all-rac-α-tocopherol), natural source vitamin E (RRR-rac-α-tocopherol) or placebo capsules and were followed up for a period of 8 weeks. Supplemented groups also received dietary guidance for an energy-restricted diet. An additional group that received no supplementation and did not follow an energy-restricted diet was also followed up. The intervention effect was evaluated by DNA methylation levels (quantitative real-time PCR assay) and anthropometric and biochemical variables (fasting plasma glucose, haemoglobin A1C, insulin, and vitamin E).ResultsIncreased methylation levels of the miR-9-3 promoter region (P < 0.001) and reduced haemoglobin A1C (P < 0.05) were observed in the natural source vitamin E group after intervention. Increased fasting plasma glucose was observed in the synthetic vitamin E group, despite the significant reduction of anthropometric variables compared to the other groups.Conclusionsα-Tocopherol from natural sources increased methylation levels of the miR-9-3 promoter region and reduced haemoglobin A1C in overweight women following an energy-restricted diet. These results provide novel information about the influence of vitamin E on DNA methylation.Trial registrationClinicalTrials.gov, NCT02922491. Registered 4 October, 2016.Electronic supplementary materialThe online version of this article (10.1186/s12986-018-0286-7) contains supplementary material, which is available to authorized users.

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“…The cause of obesity has recently been proposed to be related to complex, multifactorial biological and environmental factors ( Bell, 2017 ; O’Rahilly and Farooqi, 2000 ). From a biological point of view, obesity is known to determine physiological and genetic, race, sex, and age.…”

Section: Introductionmentioning

confidence: 99%

Lack of association between glutathione s-transferase mu 1 (GSTM1) gene polymorphisms and obesity

Yang

2017

J Exerc Rehabil

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Recent researches suggested that personal individual’s genetic background is contributed to the susceptibility to obesity. The present of this study is to investigate whether single nucleotide polymorphisms (SNPs) of glutathione s-transferase mu 1 (GSTM1) gene are susceptibility to obesity in Korean population. In present study, two SNPs (rs1056806 [Asp142Asp], rs3815029 [promoter]) of GSTM1 gene were genotyped in 117 overweight/obese subjects with a body mass index (BMI)≥23 kg/m2 and 125 nonoverweight/obese with a BMI of 18.5–23.0 kg/m2. Genotyping of two SNPs (rs1056806 and rs3815029) was determined by sequencing after polymerase chain reaction. Logistic regression models (codominant, dominant, recessive, and log-additive models) and allele analysis were used to calculate odds ratio, 95% confidence interval, and P-values. Significant association was considered at P<0.05. Tested two SNPs in GSTM1 genes did not show any significant association with obesity (rs1056806, P=0.24 in codominant 1 model; rs3815029, P=0.59 in codominant 1, P=0.09 in codominant 2, P=0.16 in dominant, P=0.09 in recessive, and P=0.07 in log-additive models). In summary, these results indicate that SNPs of GSTM1 gene did not associated with susceptibility of obesity in the Korean population.

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The Epigenomic Analysis of Human Obesity

Cited by 48 publications

References 127 publications

Cofactors As Metabolic Sensors Driving Cell Adaptation in Physiology and Disease

Cofactors As Metabolic Sensors Driving Cell Adaptation in Physiology and Disease

α-Tocopherol influences glycaemic control and miR-9-3 DNA methylation in overweight and obese women under an energy-restricted diet: a randomized, double-blind, exploratory, controlled clinical trial

Lack of association between glutathione s-transferase mu 1 (GSTM1) gene polymorphisms and obesity

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